There’s a term, the “Cafeteria Diet” (CAF) that is used in research literature to describe a diet which is high in hyper-palatable food (described in the literature as “food regularly consumed by humans, including high‐salt, high‐fat, low‐fiber, energy dense foods such as cookies, chips, and processed meats“). These foods tend to be higher carbohydrate as well.
There are quite a few studies which looked at CAF as the explanation for Metabolic Syndrome. Here’s one of the studies (Sampey, B. P., Vanhoose, A. M., Winfield, H. M., Freemerman, A. J., Muehlbauer, M. J., Fueger, P. T., Newgard, C. B. and Makowski, L. (2011), Cafeteria Diet Is a Robust Model of Human Metabolic Syndrome With Liver and Adipose Inflammation: Comparison to High‐Fat Diet. Obesity, 19: 1109-1117). The study looked at the difference between a high fat diet and the cafeteria diet.
To investigate the obesogenic and inflammatory consequences of a cafeteria diet (CAF) compared to a lard‐based 45% HFD in rodent models, male Wistar rats were fed HFD, CAF or chow control diets for 15 weeks.
Body weight increased dramatically and remained significantly elevated in CAF‐fed rats compared to all other diets. Glucose‐ and insulin‐tolerance tests revealed that hyperinsulinemia, hyperglycemia, and glucose intolerance were exaggerated in the CAF‐fed rats compared to controls and HFD‐fed rats.
The two diets were both high fat compared with the control diet. Both of the high fat diets resulted in increased body fat. The difference was that the CAF diet caused inflammation in white fat.
Although both high fat diets resulted in increased adiposity and hepatosteatosis, CAF‐fed rats displayed remarkable inflammation in white fat, brown fat and liver compared to HFD and controls.
The study indicated that the CAF was a good model of Metabolic Syndrome.
In sum, the CAF provided a robust model of human metabolic syndrome compared to traditional lard‐based HFD, creating a phenotype of exaggerated obesity with glucose intolerance and inflammation. This model provides a unique platform to study the biochemical, genomic and physiological mechanisms of obesity and obesity‐related disease states that are pandemic in western civilization today.
This is interesting since the Diet Induced Obesity (DIO) models usually work in rats by feeding the rats a High Fat diet (HFD). The study concluded that the CAF diet was actually more effective at creating the Metabolic Syndrome than the High Fat Diet (HFD).
Our study has revealed that rats fed human nutrient poor foods develop severe metabolic syndrome which is more robust than the effect of traditional HFD exposure.
The power of these sorts of studies is that that were done on ad libitum fed rats. That is, they ate as much as they wanted to eat. They did not feed the rats a diet limited in any way. They simply presented the food and measured what was left to determine what the rats ate.
This can’t be blamed on sugar since the Low Fat diet contained the most sugar. It can’t simply be blamed on carbohydrates although CAF had higher carbohydrates.
The high fat diet also had a self-regulating capacity which the CAF diet lacked. As the study noted:
…study revealed that while HFD-fed animals decreased food intake in terms of total grams to maintain caloric intake comparable to LFD and SC control, CAF-fed animals lacked this autoregulatory mechanism… CAF-fed rats were hyperphagic, eating 40% more calories/day compared to the HFD.
This may be a part of the advantage of the Low Carb High Fat diet for diabetics. To summarize:
Our study has revealed that rats fed human nutrient poor foods develop severe metabolic syndrome which is more robust than the effect of traditional HFD exposure. CAF-diet fed rats exhibited voluntary hyperphagia and grossly elevated fat intake which resulted in dramatic and rapid weight gain.
Furthermore, CAF diet feeding promoted a prediabetic condition with elevated glucose, insulin, and nonesterified fatty acids, accompanied by decreased glucose and insulin tolerance. In addition, chronically inflamed liver and adipose tissues and distorted pancreatic islet architecture were prevalent.