SummaryThere is an ecological association between total and animal fat consumption and colorectal and breast cancer risk. Mortality data for breast and colorectal cancer for 24 European countries correlated, as expected, with the consumption of animal, but not vegetable, fat. There was an inverse correlation with fish and fish oil consumption, when expressed as a proportion of total or animal fat, and this correlation was significant for both male and female colorectal cancer and for female breast cancer, whether the intakes were in the current time period, or 10 years or 23 years before cancer mortality. These effects were only seen in countries with a high (>85 g caput-1 day-l) animal fat intake. This evidence suggests that fish oil consumption is associated with protection against the promotional effects of animal fat in colorectal and breast carcinogenesis.

Detection of intestinal metaplasia is subject to significant sampling error. It increases with segment length and number of biopsies taken. In the majority of patients, if sufficient biopsies are taken over time, intestinal metaplasia will be demonstrated. The decision to offer surveillance should not be based upon the presence or absence of intestinal metaplasia at index endoscopy as the risk of dysplasia and adenocarcinoma is similar in both groups.

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Hepatocellular carcinomata are relatively rare in the western hemisphere, but they are much more common in South-East Asia and sub-Saharan Africa due to high endogenous levels of hepatitis B and C. Ectopic liver tissue usually is found incidentally (frequently at cholecystectomy), but it may also be found due to neoplastic changes or compressive effects. Ectopic liver tissue has an increased neoplastic potential over orthotopic liver, which we postulate is due to compromised vascular supply and biliary drainage. These lesions may be susceptible to surgical resection, although long-term follow-up data are poor. Ectopic or accessory liver tissue is a rare condition. Most commonly, it is found incidentally, but it may also be found as a result of neoplasia or compressive effects. These lesions appear to have an increased potential for the development of hepatocellular carcinoma in the absence of malignancy in the mother liver. Due to their anatomical features, these carcinomata appear to be susceptible to curative resection, although long-term follow-up data are poor. These carcinomata have been reported more frequently from South-East Asia than from Western countries; however, the common risk factors for hepatocellular carcinoma, such as infection with hepatitis B or C and cirrhosis, appear to be less implicated than in carcinomata of the orthotopic liver. In ectopic or accessory liver tissue, development of hepatocellular carcinoma may be the result of compromised vascular supply or biliary drainage.

SUMMARY Of 5018 patients who had undergone gastric surgery at St James Hospital, Balham, at least 25 years ago, death certificates have been received for 2768, whilst 1746 patients are still alive and are flagged (Office of Populations, Censuses and Surveys (OPCS) will notify us of their death and its cause) and only 504 could not be traced. Mortality from cancers of various organs has been determined using a 'years at risk' calculation in five year bands. There was no increase in mortality risk from any cancers during the first 15 postoperative years, but from 20 years after operation there was a significant excess risk not only of cancer of the stomach (4.5-fold), but also of the large bowel (1-6-fold), bronchus (3.9-fold), pancreas (4-0-fold), biliary tract (9-1-fold), oesophagus (2.3-fold), bladder (2-4-fold), breast (4-0-fold), and cancer of all sites (3-3-fold). These findings are consistent with the production in the operated-upon stomach of circulating carcinogens with a 20 year latency period.There have been a number of studies relating surgery for peptic ulcer to the subsequent risk of gastric cancer, some showing an association'-4 and some not."7 Many possible explanations for this have been suggested, but our large study' of 2577 duodenal ulcer patients and 1385 gastric ulcer patients showed that whereas more than 20 years postsurgery both groups of patients had an excess risk of gastric cancer, during the first 20 postoperative years there was an excess risk in the gastric ulcer patients but a decreased risk in duodenal ulcer patients. Thus, an association between gastric surgery and gastric cancer in either direction or no association at all could be expected depending solely on the relative proportion of duodenal ulcer and gastric ulcer patients, and on the length of follow up.A possible mechanism for this increased carcinogenesis is that surgery results in gastric hypoacidity leading to bacterial overgrowth with consequent production of carcinogens. A hypothesis involving nitrite and N-nitroso compounds has been sug-

The 4:1 sex ratio and 20-yr age shift between males and females in the prevalence of BE, both IM+ and IM-, found in younger age groups, was the main cause of the overall BE 2:1 sex ratio. The very similar demographics of IM- and IM+ BE suggest they may be two consecutive stages in the same metaplastic process.

The hypothesis that high nitrate ingestion may increase the risk of stomach cancer has led to concern over rising levels of nitrate in drinking water, but with little consideration as to whether nitrate from water makes a major contribution to total nitrate intake. In order to investigate the relative importance of water and food as sources of nitrate, 404 adult well-water users completed a diet diary over a 48-hour period and provided a 24-hour urine specimen and a sample of their drinking water. Where the waterborne nitrate level is less than 50 mg/I, as recommended by the World Health Organization (WHO), 30% of ingested nitrate is from water. As the well-water nitrate concentration rises the contribution of water to daily intake increases; at levels between 50 and 100 mg/I, on average, nearly 70% of daily intake is from water, and above 100 mg/I over 80% of daily intake is waterborne. Thus it is only at levels above those currently recommended by the WHO that waterborne nitrate appears to be the major contributor to total nitrate intake.