Vegetarians and vegans may be most at risk from low selenium intakes.
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Biomedical subjects
Publications and source records attributed to C P Caygill.
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There 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-1) 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.
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It has been demonstrated that bacteria can produce the very potent carcinogens (N-nitroso compounds), from nitrite and suitable amines. It has been hypothesized that this can happen whenever a body site which is normally sterile becomes colonized by bacteria. If this is so then such chronic infections should result in an increased incidence of local cancers and also of cancers at some distant sites. To test this we studied the risk of cancer at various sites in a cohort of chronic carriers of Salmonella typhi/paratyphi. We have observed a greatly increased risk of cancers of the biliary tract and also of cancers of the colorectum, pancreas, lung and all sites. The results are discussed in terms of the hypothesis being tested.
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Although there is a strong positive association between total fat consumption and colorectal and breast cancer risk, there is evidence that n-3 fatty acids, mainly found in fish oil, are protective. If this is so, we would expect to be able to detect an inverse correlation between fish consumption and colorectal cancer and breast cancer mortality. Mortality data for breast and colorectal cancer in 24 European countries were correlated with current fish and fish oil consumption and with consumption 10 and 23 years previously. In males there was an inverse correlation between colorectal cancer mortality and current intake of fish (P = 0.036), a weaker correlation with fish consumption 10 years earlier (P = 0.042) and none with consumption 23 years earlier (P = 0.12). The data were not statistically significant in females. There was no correlation at all between breast cancer mortality and fish or fish oil consumption at any time. It is concluded that fish consumption is associated with protection against the later promotional stages of colorectal carcinogenesis, but not with the early initiation stages. The results are discussed in terms of the role of prostaglandins in colorectal carcinogenesis.
It has been shown in vitro that bacteria are able to form or release carcinogens, mutagens, or promoters from intestinal secretions such as bile, or from excretions such as urine. It is, therefore, of interest to find out whether chronic infection of the gallbladder is associated with carcinogens, as in chronic infection of the urinary bladder. A study of cancer risk in chronic typhoid and paratyphoid carriers showed a large excess (observed/expected cases) for cancer of the gallbladder (167.0; 95% confidence interval 54.1-389) and also excess risks of cancer of the pancreas (8.1), colorectum (3.0), lung (2.5), and all neoplasms (2.6). There was no similar excess risk in a group of 386 people with typhoid from the 1964 Aberdeen outbreak. This indicates that it is long-term typhoid carriage, not acute infection, which is the risk factor. This has important implications for cancer prevention. Eradication of chronic carriage, by use of antibiotics or elective cholecystectomy, should be re-emphasised, and the need for good documentation of carriers is, therefore, of great importance.
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Oesophageal adenocarcinoma (which has been steadily increasing in incidence during the last 20 years) is thought to be promoted by gastric reflux. In a cohort of 5018 gastric surgery patients, 19 of whom developed oesophageal cancer, there was no increased proportion of adenocarcinomas. We conclude that the hypothesized aetiology was not supported.
Environmental factors such as diet, industrial pollution, smoking and viruses account for some 80% of cancers and more than one-quarter of all non-accidental deaths. Little attention has been paid to the relationship between bacterial infection and cancer but there is growing evidence to support this link. For some sites, such as stomach and colorectum, the evidence is relatively strong, whereas for others, such as biliary tract and bladder, it is more circumstantial.
Since 1986 there have been a number of large studies of cancer risk after surgery for benign disease involving over 20,000 patients followed for at least 20 years. All show that gastric surgery carries an excess risk of gastric cancer after a 15-20 year latency. There is less agreement about the excess risk at other sites. The size of such risks appears to depend on the size of cohort, type of ulcer, type of surgery, length of follow-up and level of analytical detail. Statistically significant excess risks have been reported for cancer of the colon (6/8 studies), biliary tract (4/5), lung (6/6), bladder (3/3), pancreas (4/7) and all sites (2/3). Our own study showed an excess risk of cancer of the gallbladder (14.3 fold), stomach (4.5), breast (4.0), bronchus (3.9), large bowel (1.6), oesophagus (2.3), pancreas (4.0), bladder (2.4) and all sites (3.3).
In this study the trends in breast cancer incidence in a number of European countries, over the last 20 years, have been evaluated. There is a wide range in incidence; the risk being highest in north and west Europe (and highest in Switzerland) and lower in south and in east Europe. There was little difference, however, between countries in the incidence of the disease occurring before the menopause, and this incidence has shown little temporal change in the time period 1960-1985. Indeed, in many countries there has been little change in incidence in any age band since 1975. The use of oral contraception has been claimed to be a risk factor in premenopausal breast cancer. In two countries, the data on oral contraceptive usage were available; in neither was there any evidence that the introduction and growth in such usage was related to the risk of breast cancer in any age band that might have been exposed to them. The reasons for this are discussed in the light of recent reports to the contrary.
Patients (1,643) undergoing vagotomy for peptic ulcer at York District Hospital were traced through the Office of Populations Censuses and Surveys (OPCS) and cause of mortality obtained for the 577 who had died. Expected mortality for the cohort was calculated using a years at risk calculation in 5 year bands. There was an excess risk of mortality from cancer of all sites (1.5-fold), stomach (1.6-fold), colorectum (1.7-fold), biliary tract (4.1-fold) and lung (1.6-fold). There was no excess risk or mortality from cancer of the oesophagus, pancreas and female breast. The numbers of deaths have been too few and length of follow-up too short to investigate latency. The findings are consistent with the production of carcinogens as a result of the hypoacidity following vagotomy.
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Evidence is presented that N-nitroso compounds occur in bile from patients who have undergone surgery for gallstones or had gastrectomy and from unoperated persons. It is unlikely, therefore, that local formation of nitrosamines can account for the excess risk for gallbladder cancer in the first two groups. Gastric formation remains the likeliest hypothesis.