As early as at the beginning of the last century, animal studies have pointed to a causal role of dietary cholesterol in atherogenesis. In humans, however, most observational studies have not provided convincing evidence for an impact of cholesterol intake on coronary heart disease (CHD). Rather, these studies have consistently established a close association between a certain eating pattern and the risk of CHD. This eating pattern has usually been characterized by a high intake of total fat, saturated fatty acids (SFA) and cholesterol, and a low intake of fiber and polyunsaturated fatty acids (PUFA). In typical western diets the amounts of total fat, SFA, and cholesterol are strongly correlated with each other, while they are negatively related to the intake of fiber and PUFA. Thus, it has not been possible to determine whether the association between the above mentioned eating pattern and CHD is due to the high consumption of SFA, cholesterol, both, or an insufficient supply of one or more protective factors such as fiber or PUFA. As the consumption of eggs leads to a high intake of cholesterol without necessarily resulting in high uptake levels of SFA and total fat, several groups have tried to elucidate the effect of cholesterol by investigating the relationship between the consumption of eggs and the development of CHD. Based on these studies, the association between dietary cholesterol and CHD risk is, if anything, minor in nature. This is consistent with the finding that an increase in dietary cholesterol intake results in only a minimal increase in the total/high-density lipoprotein cholesterol ratio. Taken together these studies suggest that the association between dietary cholesterol and CHD is small, as most subjects can effectively adapt to higher levels of cholesterol intake. Nevertheless, lowering dietary cholesterol content might reduce the risk of CHD considerably in a subgroup of individuals who are highly responsive to changes in cholesterol intake.