Cholesterol was also tested in combination with various carcinogens, but the results are insufficient to assess the co-carcinogenic potential of this compound. Cholesterol, when free of oxidation products, was not mutagenic in bacteria and did not cause cell transformation. The data were inadequate to evaluate the activity of cholesterol in short-term tests. Cholesterol induced cleft palate in rats. 5.2 Human data Cholesterol and cholesterol derivatives are widely distributed in human tissues and in the human diet.
Cholesterol is used in a multitude of pharmaceutical and cosmetic preparations.
As in the preceding presentation of epidemiological data, the evidence is summarized according to the three contexts in which cholesterol has been measured, i.e., in the diet, the blood and the faeces. Few epidemiological studies of cancer have examined dietary cholesterol specifically, although many have examined total saturated fat intake. Although there is moderately consistent, albeit limited, evidence of an association between high dietary intake of cholesterol and cancers of the colon, breast and, less convincingly, some other cancers, a causal relationship cannot be inferred from these epidemiological data. In particular, there is a difficulty in distinguishing between any effect of cholesterol and the effects of other dietary factors with which cholesterol is positively or negatively correlated. It seems clear that serum cholesterol does not have a strong or direct relationship with human carcinogenesis in general, of the kind it apparently has with coronary heart disease.