Dietary Vitamin a Deficiencies and Stomach Cancer

Stehr, Paul A.; Gloninger, Margaret F.; Kuller, Lewis H.; Marsh, Gary M.; Radford, Edward P.; Weinberg, Gene B.

doi:10.1093/oxfordjournals.aje.a113984

Cited by 34 publications

(11 citation statements)

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“…Our findings of a dose-response reduction in risk associated with increases in ingestion of carotene and certain vegetables are consistent with previous observations (25,(31)(32)(33)(34)(35)(36)(37)(38), as shown in Table 11.…”

Section: Discussionsupporting

confidence: 93%

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Diet in the epidemiology of gastric cancer

Graham¹,

Haughey²,

Marshall³

et al. 1990

Nutrition and Cancer

147

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We examined the nutritional epidemiology of gastric cancer in 293 cases and neighborhood-, age-, and sex-matched controls in communities throughout the counties of Niagara, Monroe, and Erie in western New York. The interview was highly detailed, requiring two and one-half hours to complete; it attempted to provide an estimate of total calories ingested as well as of macro- and micronutrients and behaviors that could affect alimentary exposures, such as the use of refrigeration. We found that risk was enhanced by sodium, fat, and retinol. Substantial reductions in risk were associated with ingestion of carotene, especially raw vegetables (including celery, cucumbers, carrots, green peppers, tomatoes, and onions), as well as with increased use of low-temperature food storage. Both refrigeration and carotene could inhibit oxidation products that could act as carcinogens in the stomach.

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Section: Discussionsupporting

confidence: 93%

“…Also, epidemiological inquiries found increases in risk with salt ingestion, either when studied as total ingestion of sodium in foods or when examined per specific highly salted food item. 32 Nutrition and Cancer 1990…”

Section: Discussionmentioning

confidence: 99%

Diet in the epidemiology of gastric cancer

Graham¹,

Haughey²,

Marshall³

et al. 1990

Nutrition and Cancer

147

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“…It showed no significant anti-cancer activity. Rettura and his colleagues (1982) found that beta-carotene (and retinyl (Stocks, 1958;Bjelke, 1975;Phillips, 1975;MacLennan et al, 1977;Bjelke, 1978;Tuyns et al, 1978;Cook-Mozaffari et al, 1979;Hirayama, 1979;Mettlin et al, 1979;Gregor et al, 1980;Mettlin et al, 1981;Modan et al, 1981;Shekelle et al, 1981;Kvale et al, 1983;Byers et al, 1984;Hinds et al, 1984;Ziegler et al, 1984;Long-De W. et al, 1985;Samet et al, 1985;Stehr et al, 1985;Wu et al, 1985;Pisani et al, 1986;Kolonel et al, 1987). For lung cancer, the results are clear-cut; the relative risk lying between 1.5 and 2.5 among those with low estimated betacarotene intakes compared with those with a high intake.…”

mentioning

confidence: 99%

Serum beta-carotene and subsequent risk of cancer: results from the BUPA Study

Wald

Thompson²,

Densem³

et al. 1988

Br J Cancer

133

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Summary In the BUPA Study, a prospective study of 22,000 men attending a screening centre in London, serum samples were collected and stored. The concentration of beta-carotene was measured in the stored serum samples from 271 men who were subsequently notified as having cancer and from 533 unaffected controls, matched for age, smoking history and duration of storage of the serum samples. The mean betacarotene level of the cancer subjects was significantly lower than that of their matched controls (198 and 221 Mg I1 respectively, P=0.007). The difference was apparent in subjects from whom blood was collected several years before the diagnosis of the cancer, indicating that the low beta-carotene levels in the cancer subjects were It has been suggested that beta-carotene (and other carotenoids) may play a role in reducing the incidence of cancer (Peto et al., 1981). Beta-carotene has anti-oxidant activity (Burton & Ingold, 1984); it is an efficient quencher of singlet oxygen (Foote, 1979). Singlet oxygen is a toxic, and possibly cancer inducing, form of oxygen that occurs as a result of many metabolic reactions.There is limited evidence to suggest that beta-carotene supplementation reduces the risks of chemically induced tumours in animals. Since an important function of carotenoid pigments is to protect organisms from photosensitisation, and hence probably skin cancer which can occur as a result, the administration of beta-carotene to animals is likely to reduce the incidence of skin cancers occurring in those animals. What is, perhaps, of greater interest is whether the administration of beta-carotene can reduce the incidence of cancers that are not induced by ultraviolet light, and in particular of cancers that affect tissues other than skin. Dorogokupla (cited by MathewsRoth, 1982) induced subcutaneous tumours in rats with injections of 9,10-dimethyl-1-2-benzanthracene (DMBA) and skin tumours in mice by the topical application of DMBA; animals fed a diet supplemented with unlimited amounts of red carrots developed tumours at a lower rate than did the animals receiving the unsupplemented diet. Mathews-Roth (1982) administered about 6.7 grams of beta-carotene per kilogram of diet per day to mice and showed that this led to a considerable increase in pigment accumulation in the skin (593 mg 100 g-1 skin) and that the induction of skin tumours by 7,12-dimethylbenzanthracene promoted by croton oil, was inhibited by the stored beta-carotene, there being 3.4 tumours per mouse in the beta-carotene group compared to 11.6 tumours per mouse in the control group (P<0.01). Mathews-Roth used canthaxanthin, a carotenoid without vitamin A activity, as a control substance. It showed no significant anti-cancer activity. Rettura and his colleagues (1982) found that beta-carotene (and retinyl (Stocks, 1958;Bjelke, 1975;Phillips, 1975;MacLennan et al, 1977;Bjelke, 1978;Tuyns et al., 1978;Cook-Mozaffari et al., 1979;Hirayama, 1979;Mettlin et al., 1979;Gregor et al., 1980;Mettlin et al., 1981;Modan et al., 1981;Shekelle et al....

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“…These include various agents with damaging effects on the normal gastric epithelium, as mentioned in the literature. Helicobacter pylori infection (Taylor & Blaser, 1991;Forman et al, 1994;Nightingale & Grueber, 1994;Munõz, 1994), perhaps mainly during early periods of life (Goodman & Correa, 1995), nitrosamine precursors in industrialized foods (Mirvish, 1994), and facilitating factors associated with either a salt-rich diet, alcohol intake, or deficient consumption of fresh fruits and vegetables have been mentioned as associated with stomach cancer (Antonioli, 1994;Hwang et al, 1994;Kodama et al, 1984;Risch et al, 1985;Stehr et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Stomach cancer incidence in Brazil: an ecologic study with selected risk factors

Koifman

1997

Cad. Saúde Pública

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Contrary to many industrialized countries in which a sharp decline in stomach cancer incidence has been observed, Brazil still shows intermediate to high incidence rates. An ecologic analysis was performed to explore variables possibly associated with the development of stomach cancer. Cluster analysis, principal component analysis, and factor analysis were carried out with population data, including the following: stomach cancer incidence rates in the early 1990s obtained from population-based cancer registries in Porto Alegre, Campinas, Fortaleza, Belém, and Goiânia; and data from a Brazilian national survey on family expenditures (several diet consumption items and availability of home refrigerators) carried out in 1974-75. The results suggested that past availability of a home refrigerator, i.e. food preservation, may have played an important role in currently observed differences in stomach cancer incidence among the various populations studied in Brazil. Differences in living standards among populations in these cities also appear to have played an important role in the observed incidence differences.

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Dietary Vitamin a Deficiencies and Stomach Cancer

Cited by 34 publications

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Diet in the epidemiology of gastric cancer

Diet in the epidemiology of gastric cancer

Serum beta-carotene and subsequent risk of cancer: results from the BUPA Study

Stomach cancer incidence in Brazil: an ecologic study with selected risk factors

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