Although a relationship between high-fat food and atherosclerosis was earlier suspected, an interest in the impact of lipids on health appeared only in the 1950s when dietary lipids were implicated in the genesis of cardiac atherosclerosis. The vast epidemiological study by the American chemist A. Keys (1953) established for the rst time relationships between the level of dietary lipids and mortality from cardiovascular events. In the eld of overweight and obesity studies, it appeared that in patients maintained with a normocaloric diet an increase in the proportion of fat in the diet did not necessarily lead to an increased adiposity; it may even be accompanied by weight loss (Shikany et al. 2010). These conclusions were made in 2010 by J.M. Shikany, the United States, after an analysis of 13 highly controlled studies that were achieved between 1976 and 2005. On the reverse, under conditions of low energy intake a decrease in the lipid ration induced a weight increase. Thus, in the United States, following the recommendations of nutritionists to the population, there has been a decrease in fat intake, which was nevertheless accompanied by increasingly common obesity. It is obvious that the increase in body weight is better correlated to excessive energy intake than to excessive fat intake. Lipids may obviously contribute to obesity, but they are only one factor in a complex and multifactorial process. It is therefore easy to understand why ghting obesity cannot be reduced to limiting fat intakes. It must be necessary rst to restrict the energy sources contained in the plate and to increase energy expenditure by an appropriate physical activity.