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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review of the scientific literature on the relationship between vegetable and fruit consumption and risk of cancer, results from 206 human epidemiologic studies and 22 animal studies are summarized. The evidence for a protective effect of greater vegetable and fruit consumption is consistent for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon. The types of vegetables or fruit that most often appear to be protective against cancer are raw vegetables, followed by allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes. Substances present in vegetables and fruit that may help protect against cancer, and their mechanisms, are also briefly reviewed; these include dithiolthiones, isothiocyanates, indole-3-carbinol, allium compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene, lycopene, selenium, vitamin E, flavonoids, and dietary fiber. Current US vegetable and fruit intake, which averages about 3.4 servings per day, is discussed, as are possible noncancer-related effects of increased vegetable and fruit consumption, including benefits against cardiovascular disease, diabetes, stroke, obesity, diverticulosis, and cataracts. Suggestions for dietitians to use in counseling persons toward increasing vegetable and fruit intake are presented.
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PMID:Vegetables, fruit, and cancer prevention: a review. 884 Nov 65

Agents known or believed to be carcinogenic decrease the concentration of potassium and increase the concentration of sodium in the cells. Anticarcinogenic agents have the opposite effect. In all cases where we have information on an agent's carcinogenicity or anticarcinogenicity and on that agent's effects on cellular potassium and sodium concentrations the above relationships have been found to be true. Dietary carcinogenic agents studied include sodium, cadmium, fat, cholesterol, calories, and alcohol; dietary anticarcinogenic agents include potassium, vitamins A, C, and D, selenium, and fiber. The effect of calcium intake is less clear as that effect depends on the concentrations on sodium and potassium. Not only dietary agents but also other carcinogenic and anticarcinogenic agents work in the same way. The cancer-causing drug dimethylhydrazine increases sodium and decreases potassium in the cells, whereas, for example, indomethacin, an anticarcinogen, has the opposite effect. In aging potassium leaves the cells, sodium enters them, and the rates of cancer increase. Patients with hyperkalemic diseases (Parkinson, Addison) have reduced cancer rates, and patients with hypokalemic diseases (alcoholism, obesity, stress) have increased cancer rates.
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PMID:Potassium, sodium, and cancer: a review. 921 87

Nutrition is a critical determinant of immune responses and malnutrition the most common cause of immunodeficiency worldwide. Protein-energy malnutrition is associated with a significant impairment of cell-mediated immunity, phagocyte function, complement system, secretory immunoglobulin A antibody concentrations, and cytokine production. Deficiency of single nutrients also results in altered immune responses: this is observed even when the deficiency state is relatively mild. Of the micronutrients, zinc; selenium; iron; copper; vitamins A, C, E, and B-6; and folic acid have important influences on immune responses. Overnutrition and obesity also reduce immunity. Low-birth-weight infants have a prolonged impairment of cell-mediated immunity that can be partly restored by providing extra amounts of dietary zinc. In the elderly, impaired immunity can be enhanced by modest amounts of a combination of micronutrients. These findings have considerable practical and public health significance.
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PMID:Nutrition and the immune system: an introduction. 925 Jan 33

In the present case-control study several dietary and nutritional factors were investigated to determine if a relationship exists between diet and development of mammary tumors in female dogs. Control female dogs (n = 86) were compared with a case group of dogs (n = 102) with dysplasias or tumors of the mammary gland. A questionnaire providing information on the dog's body conformation and dietary and reproductive histories was answered by the owners. Serum selenium and retinol concentrations and the fatty acid profile in subcutaneous adipose tissue were analyzed as indicators of nutritional status. Obesity at 1 year of age and 1 year before the diagnosis of mammary nodules was found to be significantly related to a higher prevalence of mammary tumors and dysplasias. The intake of homemade meals (compared to that of commercial foods) was also significantly related to a higher incidence of tumors and dysplasias. Other significant risk factors were a high intake of red meat, especially beef and pork, and a low intake of chicken. The subcutaneous fatty acid profile and the serum selenium concentration were not significantly different in the cases and the controls, with the exception of C18:1 fatty acid (oleic acid) content, which was significantly higher in the cases than in healthy controls. Serum retinol concentration was significantly lower in the cases than in the controls. In the multivariate analysis, older age, obesity at 1 year of age, and a high red meat intake were independently and significantly associated with the risk of developing mammary tumor and dysplasias.
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PMID:Relation between habitual diet and canine mammary tumors in a case-control study. 959 73

To investigate how cigarette smoking increases the risk of cardiovascular disease, risk factors were compared between 166 cigarette smokers and 312 non-smokers, in a random sample of males (Chinese, Malays and Asian Indians) aged 30-69 years from the general population of Singapore. There was adjusted for age and ethnic group. The prevalence of hypertension was lower in cigarette smokers (15.2%) than non-smokers (21.9%), with the difference reduced by adjustment for body mass index (BMI). Smokers had: lower mean serum HDL-cholesterol (0.76 versus 0.81 mmol/l) and higher mean serum fasting triglyceride (1.92 versus 1.71 mmol/l), which will increase atherosclerosis; higher mean plasma fibrinogen (2.75 versus 2.67 g/l) and plasminogen activator inhibitor 1 [PAI-1] (24.9 versus 22.2 ng/ml), which will increase thrombosis; and lower mean plasma vitamin C (4.4 versus 6.4 mg/l) and serum selenium (118 versus 123 microg/l), which may increase atherosclerosis. Adjustment for BMI slightly increased the differences for HDL-cholesterol, fasting triglyceride, fibrinogen and PAI-1, indicating that less generalised obesity among smokers reduces their increased cardiovascular disease risk. Smoking was not found to be related to: diabetes mellitus; serum total cholesterol, LDL-cholesterol, apolipoproteins A1 and B and lipoprotein(a); plasma factor VIIc and prothrombin fragment 1 + 2; and plasma vitamins A and E and serum ferritin. There was no evidence of increased insulin resistance in smokers, as measured by mean fasting serum insulin.
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PMID:Cardiovascular risk factors in relation to cigarette smoking: a population-based survey among Asians in Singapore. 962 68

Twenty-nine obese female Zucker rats (fa/fa) were fed with a laboratory chow supplemented or not with a selenium-rich yeast (Selenion), or Selenion + vitamin E, or vitamin E alone. Twelve lean female Zucker rats (Fa/Fa) of the same littermates fed with the same diet were used as control. After 32 wk of diet, obesity induced a large increase in plasma insulin and lipid levels. A significant decrease in the plasma vitamin E/triglycerides ratio (p<0.005) and an increase in plasma thiobarbituric reactive substances (TBARS) (p<0.005) were also observed. Plasma selenium and vitamin E increased in all supplemented rats. The plasma insulin level was decreased by selenion supplementation and the vitamin E/triglycerides ratio was completely corrected by double supplementation with Selenion + vitamin E. TBARS were also efficiently decreased in two obese groups receiving vitamin E. In plasma, adipose tissue and aorta, obesity induced an increase in palmitic acid (C16:0), a very large increase in monounsaturated fatty acids (palmitoleic acid C16:1, stearic acid C18:1) associated with a decrease in polyunsaturated n-6 fatty acids (linoleic acid C18:2 n-6, arachidonic C20:4 n-6). These alterations in fatty acid distribution were only partly modulated by Se and vitamin E supplements. However, in the aorta, antioxidant treatment in obese rats significantly reduced the increase in C16:0 and C16:1 (p<0.05 and p<0.01, respectively) and the decrease in arachidonic acid (p<0.05). These changes could be beneficial in the reduction of insulin resistance and help to protect the vascular endothelium.
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PMID:Effect of selenium and vitamin E supplementation on lipid abnormalities in plasma, aorta, and adipose tissue of Zucker rats. 989 95

Thanks to progress in zinc research, it is now possible to describe in more detail how zinc ions (Zn++) and nitrogen monoxide (NO), together with glutathione (GSH) and its oxidized form, GSSG, help to regulate immune responses to antigens. NO appears to be able to liberate Zn++ from metallothionein (MT), an intracellular storage molecule for metal ions such as zinc (Zn++) and copper (Cu++). Both Zn++ and Cu++ show a concentration-dependent inactivation of a protease essential for the proliferation of the AIDS virus HIV-1, while zinc can help prevent diabetes complications through its intracellular activation of the enzyme sorbitol dehydrogenase (SDH). A Zn++ deficiency can lead to a premature transition from efficient Th1-dependent cellular antiviral immune functions to Th2-dependent humoral immune functions. Deficiencies of Zn++, NO and/or GSH shift the Th1/Th2 balance towards Th2, as do deficiencies of any of the essential nutrients (ENs) - a group that includes methionine, cysteine, arginine, vitamins A, B, C and E, zinc and selenium (Se) - because these are necessary for the synthesis and maintenance of sufficient amounts of GSH, MT and NO. Via the Th1/Th2 balance, Zn++, NO, MT and GSH collectively determine the progress and outcome of many diseases. Disregulation of the Th1/Th2 balance is responsible for autoimmune disorders such as diabetes mellitus. Under Th2, levels of interleukin-4 (II-4), II-6, II-10, leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) are raised, while levels of II-2, Zn++, NO and other substances are lowered. This makes things easier for viruses like HIV-1 which multiply in Th2 cells but rarely, if ever, in Th1 cells. AIDS viruses (HIVs) enter immune cells with the aid of the CD4 cell surface receptor in combination with a number of co-receptors which include CCR3, CCR5 and CXCR4. Remarkably, the cell surface receptor for LTB4 (BLTR) also seems to act as a co-receptor for CD4, which helps HIVs to infect immune cells. The Th2 cytokine II-4 increases the number of CXCR4 and BLTR co-receptors, as a result of which, under Th2, the HIV strains that infect immune cells are precisely those that are best able to accelerate the AIDS disease process. The II-4 released under Th2 therefore not only promotes the production of more HIVs and the rate at which they infect immune cells, it also stimulates selection for the more virulent strains. Zn++ inhibit LTB4 production and numbers of LTB4 receptors (BLTRs) in a concentration-dependent way. Zn++ help cells to keep their LTB4 'doors' shut against the more virulent strains of HIV. Moreover, a sufficiency of Zn++ and NO prevents a shift of the Th1/Th2 balance towards Th2 and thereby slows the proliferation of HIV, which it also does by inactivating the HIV protease. Research makes it look likely that deficiencies of ENs such as zinc promote the proliferation of Th2 cells at the expense of Th1 cells. Zinc deficiency also promotes cancer. Under the influence of Th1 cells, zinc inhibits the growth of tumours by activating the endogenous tumour-suppressor endostatin, which inhibits angiogenesis. The modern Western diet, with its excess of refined products such as sugar, alcohol and fats, often contains, per calorie, a deficiency of ENs such as zinc, selenium and vitamins A, B, C and E, which results in disturbed immune functions, a shifted Th1/Th2 balance, chronic (viral) infections, obesity, atherosclerosis, autoimmunity, allergies and cancer. In view of this, an optimization of dietary composition would seem to give the best chance of beating (viral) epidemics and common (chronic) diseases at a realistic price.
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PMID:Modern diets and diseases: NO-zinc balance. Under Th1, zinc and nitrogen monoxide (NO) collectively protect against viruses, AIDS, autoimmunity, diabetes, allergies, asthma, infectious diseases, atherosclerosis and cancer. 1049 17

As in many other countries, the New Zealand Cancer Society produces guidelines for cancer prevention. These recommend avoiding asbestos, smoking, sunlight, alcohol, fatty food and obesity. Women are advised to have a regular cervical smear test. Additional 'probably helpful' suggestions include eating plenty of fresh fruit and vegetables and dietary fibre. However, considerable data from animal studies and more slowly accumulating data from human intervention studies suggest additional and more specific advice may be appropriate. Fruit and vegetable servings should total a minimum of five each day. Some specific fruits and vegetables (e.g., tomato, broccoli, onions) may have particular benefits against individual cancer types. Positive human evidence on potential benefits of increasing dietary fibre comes from studies where wheat bran was added to the diet. This is not a dietary fibre per se, but merely a good fibre source. Indeed, our own studies suggest that it could be various phytochemicals in the bran, rather than dietary fibre, which is beneficial. An increase either in whole wheat or wheat bran, rather than fibre, would be a sounder recommendation. Although there is some evidence that multivitamin supplementation can protect against cancer, this may be only in the special situation where the population is already significantly vitamin-deficient. For example, a combination of beta-carotene, vitamin E and selenium significantly reduced cancer mortality in a Chinese population, whereas lung cancer risks (in already high risk groups) were increased in Finnish and American trials with high dose beta-carotene. Various other chemopreventive drugs are being actively developed and at various stages in clinical trials. The enhanced cancer incidence in the beta-carotene trial illustrates the potential benefit of utilising surrogate endpoints of malignant disease rather than incident cancer as a trial endpoint.
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PMID:Prospects for cancer prevention. 1051 4

Thirty-seven dilated cardiomyopathy cases have been studied and compared with 20 normal controls. Serum selenium levels in relation to coronary risk factors were studied. Serum samples were analysed for selenium, total cholesterol, high density lipoprotein(HDL) cholesterol, triglycerides and glucose levels. Smoking, alcohol intake, positive family history, psychosocial tension, obesity, hypercholesterolaemia, hypertriglyceridaemia and hyperglycaemia were found in the following percentages 27%, 8%, 5%, 73%, 41%, 38%, 81%, 46% respectively in dilated cardiomyopathy patients. Low selenium (< 4.5 micrograms/dl) and HDL cholesterol levels and high total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol and glucose levels were observed in dilated cardiomyopathy cases compared to controls. The present results support the concept that low selenium levels along with other risk factors play an important role in developing dilated cardiomyopathy.
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PMID:Selenium levels in dilated cardiomyopathy. 1101 77

Nitric oxide (NO) produced by the endothelium of cerebral arterioles is an important mediator of endothelium-dependent vasodilation (EDV), and also helps to prevent thrombosis and vascular remodeling. A number of risk factors for ischemic stroke are associated with impaired EDV, and this defect is usually at least partially attributable to a decrease in the production and/or stability of NO. These risk factors include hypertension, high-sodium diets, homocysteine, diabetes, visceral obesity, and aging. Conversely, many measures which may provide protection from ischemic stroke - such as ample dietary intakes of potassium, arginine, fish oil, and selenium - can have a favorable impact on EDV. Protection afforded by exercise training, estrogen replacement, statin drugs, green tea polyphenols, and cruciferous vegetables may reflect increased expression of the endothelial NO synthase. IGF-I activity stimulates endothelial NO production, and conceivably is a mediator of the protection associated with higher-protein diets in Japanese epidemiology and in hypertensive rats. These considerations prompt the conclusion that modulation of NO availability is a crucial determinant of risk for ischemic stroke. Multifactorial strategies for promoting effective cerebrovascular NO activity, complemented by measures that stabilize platelets and moderate blood viscosity, should minimize risk for ischemic stroke and help maintain vigorous cerebral perfusion into ripe old age. The possibility that such measures will also diminish risk for Alzheimer's disease, and slow the normal age-related decline in mental acuity, merits consideration. A limited amount of ecologic epidemiology suggests that both stroke and senile dementia may be extremely rare in cultures still consuming traditional unsalted whole-food diets. Other lines of evidence suggest that promotion of endothelial NO activity may decrease risk for age-related macular degeneration.
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PMID:Up-regulation of endothelial nitric oxide activity as a central strategy for prevention of ischemic stroke - just say NO to stroke! 1105 18


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