Looking at the structure of the article, it starts by mentioning a study, and then it jumps to some advice and recipes from an unrelated nutritionist. To my eye, it doesn't even appear as though the nutritionist is responding to the study.
So what did the study say? I confess, I didn't read it. But I found the press release (which tend to be much closer to the original study than reports on science in a
cookbook daily newspaper, but could still contain misleading information.)
The press release was from March 2010, and talks about an upcoming publication in the International Journal of Obesity.
[It] examined the influence exerted by the type of foods and specific timing of intake on the development of metabolic syndrome characteristics in mice. The UAB research revealed that mice fed a meal higher in fat after waking had normal metabolic profiles. In contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome.
Bray and Young said further research needs to test whether similar observations are made with different types of dietary fats and carbohydrates, and it needs to be tested in humans to see if the findings are similar between rodents and humans.
"We're also working on a study right now to determine if these feeding regimens adversely affect heart function," Young said.
Note: They weren't studying the difference between high-fat in the morning versus low-fat in the morning (e.g. fry-up versus toast) but high-fat in the morning versus high-fat in the evening (e.g. do you eat toast for breakfast and a fry-up for dinner, or a fry-up for breakfast and toast for dinner.)
So, an intriguing study in mice, a year ago, but not yet understood nor tested in humans gave the Daily Mail (and other newspapers) an excuse to publish some recipes.
Int J Obes (Lond). 2010 Nov;34(11):1589-98. Epub 2010 Mar 30.
Time-of-day-dependent dietary fat consumption influences multiple cardiometabolic syndrome parameters in mice.
Bray MS, Tsai JY, Villegas-Montoya C, Boland BB, Blasier Z, Egbejimi O, Kueht M, Young ME.
Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Excess caloric intake is strongly associated with the development of increased adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hyperleptinemia (that is the cardiometabolic syndrome). Research efforts have focused attention primarily on the quality (that is nutritional content) and/or quantity of ingested calories as potential causes for diet-induced pathology. Despite growing acceptance that biological rhythms profoundly influence energy homeostasis, little is known regarding how the timing of nutrient ingestion influences development of common metabolic diseases.
To test the hypothesis that the time of day at which dietary fat is consumed significantly influences multiple cardiometabolic syndrome parameters.
We report that mice fed either low- or high-fat diets in a contiguous manner during the 12 h awake/active period adjust both food intake and energy expenditure appropriately, such that metabolic parameters are maintained within a normal physiologic range. In contrast, fluctuation in dietary composition during the active period (as occurs in human beings) markedly influences whole body metabolic homeostasis. Mice fed a high-fat meal at the beginning of the active period retain metabolic flexibility in response to dietary challenges later in the active period (as revealed by indirect calorimetry). Conversely, consumption of high-fat meal at the end of the active phase leads to increased weight gain, adiposity, glucose intolerance, hyperinsulinemia, hypertriglyceridemia, and hyperleptinemia (that is cardiometabolic syndrome) in mice. The latter perturbations in energy/metabolic homeostasis are independent of daily total or fat-derived calories.
The time of day at which carbohydrate versus fat is consumed markedly influences multiple cardiometabolic syndrome parameters.