I haven't readed the whole thing nor can find now the sections which can help you the most, some extractions noneless:
" Higher total fat diets can probably be consumed safely by active individuals while maintaining body weight. Although in longitudinal studies of weight gain, where dietary fat predicts weight gain independent of physical activity, it is important to note that physical activity may account for a greater percentage of the variance in weight gain than does dietary fat (Hill et al., 1989). Another endpoint that merits consideration is physical performance. High fat diets (69 percent of energy) do not appear to compromise endurance in trained athletes (Goedecke et al., 1999); however, athletes may not be able to train as effectively on short-term (less than 6 days) intakes of a high fat diet as on a high carbohydrate diet (Helge, 2000). This effect on training was not observed following long-term adaptation of high fat diets."
"As shown in Tables 9-5 through 9-8, no consistent significant associations have been established between dietary cholesterol intake and cancer, including lung, breast, colon, and prostate"
"The lack of consistency in observations relating dietary cholesterol intake to clinical cardiovascular disease and CHD endpoints may be due to many factors, including the limited ability to detect such effects (e.g., due to relatively small increases in LDL cholesterol concentration and inaccuracies in dietary intake data) and to the limited ability to distinguish the effects of dietary cholesterol independent of energy intake and other dietary variables that may be positively (e.g., saturated fat intake) or negatively (e.g., fiber intake) associated with dietary cholesterol and heart disease risk. Another uncertainty relates to interpreting the effects of dietary cholesterol on blood cholesterol concentrations. Evidence indicates that increased dietary cholesterol results, on average, in increased blood concentrations of both LDL and HDL cholesterol, and it is possible that the net impact on cardiovascular disease risk depends on the relative changes in these lipoproteins, as well as on other unmeasured mediators of atherogenesis. Finally, the considerable interindividual variation in lipid response to dietary cholesterol may result in differing outcomes in different populations or population subgroups."
"However, a number of other epidemiological studies have not demonstrated a significant independent relationship of dietary cholesterol intake and CHD (Esrey et al., 1996; Kromhout and de Lezenne Coulander, 1984; Pietinen et al., 1997; Posner et al., 1991). In a cohort of 43,757 male health professionals, dietary cholesterol intake was significantly related to age-adjusted risk for myocardial infarction and fatal CHD (p < 0.003 and 0.002, respectively) across cholesterol quintiles ranging from median intakes of 189 to 422 mg/d (Ascherio et al., 1996). However, the risk was attenuated with multivariate analyses (p < 0.07 and 0.03), which included other risk factors such as body mass index, smoking habits, alcohol consumption, physical activity, history of hypertension or high blood cholesterol, family history of myocardial infarction, and profession. The risk became insignificant after adjustment for fiber intake, which was reported to be significantly inversely related to CHD risk in this cohort."