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

Data from epidemiologic, experimental, and animal studies indicate that diet plays an important role in the etiology of gastric cancer. High intake of fresh fruits and vegetables, lycopene and lycopene-containing food products, and potentially vitamin C and selenium may reduce the risk for gastric cancer. Data also suggest that high intake of nitrosamines, processed meat products, salt and salted foods, and overweight and obesity are associated with increased risk for gastric cancer. However, current data provide little support for an association of beta-carotene, vitamin E, and alcohol consumption with risk for gastric cancer.
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PMID:Nutrition and gastric cancer risk: an update. 1845 10

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. Raised blood pressure (BP), cholesterol and smoking, are the major risk factors. Among these, raised BP is the most important cause, accounting for 62% of strokes and 49% of coronary heart disease. Importantly, the risk is throughout the range of BP, starting at systolic 115 mm Hg. There is strong evidence that our current consumption of salt is the major factor increasing BP and thereby CVD. Furthermore, a high salt diet may have direct harmful effects independent of its effect on BP, for example, increasing the risk of stroke, left ventricular hypertrophy and renal disease. Increasing evidence also suggests that salt intake is related to obesity through soft drink consumption, associated with renal stones and osteoporosis and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to food by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake, for example, Japan (1960-1970), Finland (1975 onwards) and now the United Kingdom. The challenge is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.
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PMID:A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. 1972 26

The prevalence of gastroesophageal reflux disease (GERD) ranges from 2.5% to 7.1% in most population-based studies in Asia. There is evidence that GERD and its complications are rising, coinciding with a decline in Helicobacter pylori (H. pylori) infection. Asian GERD patients share similar risk factors and pathophysiological mechanisms with their Western counterparts. Possible causes for the lower prevalence of GERD include less obesity and hiatus hernia, a lesser degree of esophageal dysmotility, a high prevalence of virulent strains of H. pylori, and low awareness. Owing to the lack of precise translation for 'heartburn' in most Asian languages, reflux symptoms are often overlooked or misinterpreted as dyspepsia or chest pain. Furthermore, a symptom-based diagnosis with a therapeutic trial of the proton pump inhibitor (PPI) may be hampered by the high prevalence of H. pylori-related disease. The risk stratification for prompt endoscopy, use of a locally-validated, diagnostic symptom questionnaire, and response to H. pylori'test and treat' help improve the accuracy of the PPI test for diagnoses. PPI remain the gold standard treatment, and 'on-demand' PPI have been shown to be a cost-effective, long-term treatment. The clinical course of GERD is benign in most patients in Asia. The risk of progression from non-erosive reflux disease to erosive esophagitis is low, and treatment response to a conventional dose of PPI is generally higher. Although H. pylori eradication may lead to more resilient GERD in a subset of patients, the benefits of H. pylori eradication outweigh the risks, especially in Asian populations with a high incidence of gastric cancer.
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PMID:Gastroesophageal reflux disease: an Asian perspective. 1912 Aug 71

Recent epidemiologic studies have shown a positive association between obesity and certain cancers. Our retrospective studies show that hypertriglyceridemia is an independent risk factor for the development of colonic adenoma and nodal metastasis in early gastric and esophageal cancer in men. High-fat condition may be favorable for the growth of malignant cells. Serum level of adiponectin is reduced in patients with advanced gastric cancer, which may be associated with the positive link between adiposity and cancer. In early gastric cancer, patients with undifferentiated type have lower fat volume than those with differentiated type. Adiposity appears to be closely related with various aspects in pathophysiology of gastrointestinal malignancy.
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PMID:Adiposity and gastrointestinal malignancy. 1915 87

Orlistat, an anti-obesity drug, is a potent inhibitor of fatty acid synthase (FAS) and tumor cell viability. It can also induce apoptotic cancer cell death. We examined the effects of Orlistat on cultured NUGC-3 gastric cancer cells. We identified that inhibition of FAS via Orlistat exposure results in rapid cellular damage preceded by a direct but short-lived autophagic response. The Orlistat induced damage can be reversed through the addition of lipid containing media in a process that normally leads to cell death. By limiting exogenous lipid availability and inhibiting FAS using Orlistat, we demonstrated both a greater sensitivity and amplified cancer cell death by activation of apoptosis. We have identified "windows of opportunity" at which time apoptosis can be aborted and cells can be reversed from the death pathway. However, when challenged beyond the window of recovery, cell death becomes all but certain as the ability to be rescued decreases considerably. In vivo examination of Orlistat's ability to inhibit gastrointestinal cancer was examined using heterozygous male C57BL/6J APC-Min mice, which spontaneously develop a fatal gastrointestinal cancer. Mice were fed either a high fat (11%) or low fat (1.2%) diet containing no Orlistat or 0.5 mg Orlistat/g of chow. Orlistat treated mice fed the high fat, but not low fat diet, survived 7-10% longer than the untreated controls.
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PMID:Inhibition of fatty acid synthase by Orlistat accelerates gastric tumor cell apoptosis in culture and increases survival rates in gastric tumor bearing mice in vivo. 1938 3

The relationship between excess body weight and gastric cancer risk has not been well studied to date. We therefore carried out a systematic review and meta-analysis of published cohort studies to evaluate the association between excess body weight and gastric cancer risk. An electronic search of the MEDLINE, PubMed, EMBASE and Academic Search Premier (EBSCO) databases, which contain articles published from 1950 onwards, was conducted in order to select studies for this meta-analysis. Ten studies with a total number of 9492 gastric cancer cases and a studied population of 3,097,794 were identified. Overall, excess body weight [body mass index (BMI)25] was associated with an increased risk of gastric cancer [odds ratio (OR)=1.22; 95% confidence intervals (CIs)=1.06-1.41]. Specifically, a stratified analysis showed that excess body weight was associated with an increased risk of cardia gastric cancer [overweight and obese (BMI 25), OR=1.55, 95% CIs=1.31-1.84] and gastric cancer among non-Asians (overweight and obese, OR=1.24, 95% CIs=1.14-1.36); however, the stratified analysis also showed that there was no statistically significant link between excess body weight and gastric cancer in the following subgroups: males (overweight and obese, OR=1.22, 95% CIs=0.96-1.55), females (overweight and obese, OR=1.13, 95% CIs=0.65-1.94), non-cardia gastric cancer (overweight and obese, OR=1.18, 95% CIs=0.96-1.45) and Asians (overweight and obese, OR=1.17, 95% CIs=0.88-1.56). The combined results of this meta-analysis, however, do indicate that overweight and obesity are associated with an increased risk of gastric cancer. The strength of the association also increases with increasing BMI.
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PMID:Overweight, obesity and gastric cancer risk: results from a meta-analysis of cohort studies. 1942 97

Adiponectin is a peptide hormone secreted from the adipose tissue, affecting the proliferation and insulin sensitivity in different cell types. The levels of adiponectin have been found to be decreased in hyperinsulinemia and insulin resistant states, such as obesity. The previous studies have suggested that plasma adiponectin levels are decreased in patients with endometrial and breast cancer. In our study, the relationship among serum adiponectin levels, demographic features and histopathological variables was evaluated in gastric cancer patients. Forty consecutive patients with gastric cancer who underwent gastrectomy with standard lymph node dissection were included and 43 healthy controls were included in this study. The serum levels of glucose, insulin, C-peptide, HbA1c and adiponectin were measured in both groups. We analyzed the correlation among these parameters and patients' demographic features, such as age, gender, body mass index (BMI) and histopathological variables such as tumor localization, stage, nodal status, histological grade, vascular and lymphatic invasion. The mean age was 60.05+9.72 in patients, while it was 38.6+12.73 in controls. The mean serum adiponectin levels were 12.62+7.9 and 10.07+6.72 ng/ml, respectively, in groups. There was no different in terms of adiponectin, C-peptide, HOMA-R level in both groups. On the other hand, BMI, glucose and insulin levels were significantly different in gastric cancer patients in comparison with the controls. There was no correlation among the levels of adiponectin, BMI, insulin and c-peptide levels in patient group (P>0.05). The adiponectin levels of woman were significantly lower than male patients (P=0.002). No relations were detected among tumor stage, tumor localization, nodal status, lymphatic and vascular invasion, and the levels of serum adiponectin (P>0.05). Interestingly, a positive correlation was found between tumor grade and plasma adiponectin levels (r=0.372; P=0.018). Our results suggest that plasma adiponectin levels were similar in both patients with gastric cancer and the controls. In addition, no correlation was found between adiponectin levels and demographic features and histopathological variables of patients. But, in undifferentiated tumors, plasma adiponectin level was significantly higher than well-differentiated grade tumors.
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PMID:The association of serum adiponectin levels with histopathological variables in gastric cancer patients. 2001 20

Raised blood pressure is a major cause of cardiovascular disease, responsible for 62% of stroke and 49% of coronary heart disease. There is overwhelming evidence that dietary salt is the major cause of raised blood pressure and that a reduction in salt intake lowers blood pressure, thereby, reducing blood pressure-related diseases. Several lines of evidence including ecological, population, and prospective cohort studies, as well as outcome trials, demonstrate that a reduction in salt intake is related to a lower risk of cardiovascular disease. Increasing evidence also suggests that a high salt intake may directly increase the risk of stroke, left ventricular hypertrophy, and renal disease; is associated with obesity through soft drink consumption; is related to renal stones and osteoporosis; is linked to the severity of asthma; and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to foods by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake. The challenge now is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.
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PMID:Reducing population salt intake worldwide: from evidence to implementation. 2022 55

Descriptive epidemiology, particularly regarding the cancer pattern in Japanese and Koreans in the United States, indicates that lifestyle factors contribute substantially to the development of common cancers such as gastric, colorectal, breast and prostate cancers. Sex and age are important determinants of many cancers, and the variation in cancer incidence according to these factors is also indicative of the role of environmental factors. While cancer of first-degree relatives or parental cancer was related to an approximately 2-fold increased risk for most site-specific cancers, a large Scandinavian twin study suggested that the contribution of genetic factors was generally small and that a statistically significant effect of hereditable factors was observed only for prostate, colorectal and breast cancers. It was roughly estimated in this article that infectious agents contributed to 20% of incident cases of cancer in Japan. In a recent cohort study in Japan, it is estimated that 29% of male cancers and 3% of female cancers can be ascribed to smoking. Among other lifestyle factors, alcohol consumption and obesity have provided convincing evidence as factors conferring increased risks of various cancers. The increased risks of colorectal cancer and breast cancer associated with alcohol drinking have been recently acknowledged internationally. Among dietary factors, red meat, aflatoxin and beta-carotene are considered to increase risks of colorectal, liver and lung cancers, respectively. Vegetables and fruits probably decrease the risk of cancer at various sites, and calcium specifically decreases the risk of colorectal cancer. Evidence for increased risk of gastric cancer associated with salted foods is judged to be not sufficient, although a high-salt diet enhanced gastric cancer in animals infected with Helicobacter pylori. The role of dietary factors in cancer development will be more clearly established by research on gene-environment interaction focusing on functional genetic polymorphisms.
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PMID:[Host and environmental factors predisposing to cancer development]. 2041 9

Besides cardiovascular disease, a high salt intake causes other adverse health effects, i.e., gastric and some other cancers, obesity (risk factor for many cancer sites), Meniere's disease, worsening of renal disease, triggering an asthma attack, osteoporosis, exacerbation of fluid retention, renal calculi, etc. Diets containing high amounts of food preserved by salting and pickling are associated with an increased risk of cancers of the stomach, nose and throat. Because gastric cancer is still the most common cancer in some countries (especially in Japan), its prevention is one of the most important aspects of cancer control strategy. Observations among Japanese immigrants in the U.S.A. and Brazil based on the geographic differences, the trend in cancer incidence with time, and change in the incidence patterns indicate that gastric cancer is closely associated with dietary factors such as the intake of salt and salted food. The findings of many epidemiological studies suggest that high dietary salt intake is a significant risk factor for gastric cancer and this association was found to be strong in the presence of Helicobacter (H.) pylori infection with atrophic gastritis. A high-salt intake strips the lining of the stomach and may make infection with H. pylori more likely or may exacerbate the infection. Salting, pickling and smoking are traditionally popular ways of preparing food in Japan and some parts of Asia. In addition to salt intake, cigarette smoking and low consumption of fruit and vegetables increase the risk of stomach cancer. However, it is not known whether it is specifically the salt in these foods or a combination of salt and other chemicals that can cause cancer. One study identified a mutagen in nitrite-treated Japanese salted fish, and chemical structure of this mutagen suggests that it is derived from methionine and that salt and nitrite are precursors for its formation. Working under conditions of heat stress greatly increased the workers' salt excretion through perspiration. Workers exposed to heat stress consumed as much as 13-38 g salt daily. As salt strongly enhances and promotes chemical gastric carcinogenesis and H. pylori infection in both humans and animals, there is an association between work, salt intake, and development of stomach cancer. Reducing salt intake, especially during pregnancy, also reduces the risk of developing breast cancer and many other diseases, as well as obesity. The risk of most cancers is reduced by losing weight. The geographical data and analyses currently available suggest that road salt (road salting in winter) may be associated with elevated mortality from cancer of the breast, lung, esophagus, throat, larynx, large intestine, rectum and bladder. There is no available literature on the health impacts of road salt. The cause and effect relationships cannot be established without further studies.
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PMID:[Salt and cancer]. 2064 83


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